During early postnatal development the chemical phenotype (i.e. neurotransmitter, peptide, receptors and ionic channels) of neurons in brain areas involved in regulation of respiration and initiation of and recovery from apnea undergoes considerable change. Disruption of these developmental patterns as a result of an abnormal environmental condition (eg hypoxia) during gestation or early postnatal life might lead to neuronal dysfunction and consequently life threatening mechanisms responsible for the Sudden Infant Death Syndrome. Upper airway patency is essential for normal respiration and specific pathologic markers of SIDS indicate upper airway obstruction as a common mode of death in SIDS victims suggesting that an animal model demonstrating perturbations of upper airway development will provide new insights into the pathophysiology of SIDS. Molecular mechanisms that mediate tissue-specific regulation of cell phenotype during development are unknown. An excellent model for study is the disappearance of somatostatin (SOM) and its mRNA in the hypoglossal nucleus (nXII) during the first month in the rat. Acetylcholine and calcitonin gene-related peptide (CGRP) are present in nXII motoneurons throughout development. We hypothesize that SOM and CGRP gene expression in nXII motoneurons modulate acetylcholine receptor maturation in the genioglossus muscle. The Specific Aims of this first study are: 1) To determine molecular factors affected by pre- and postnatal hypoxia that change temporal- and tissue-specific transcription of nXII motoneuron SOM and CGRP during early postnatal development. 2) To identify cis-elements and trans-acting protein factors that confer developmental regulation of the SOM gene in the hypoglossal neurons under conditions of normoxia and hypoxia. And, 3) to determine the trophic role of SOM in regulation of acetylcholine receptor subunit gene expression in genioglossus muscle during development in normoxia and hypoxia. Our preliminary data also indicate that gestational and postnatal hypoxia directly affects electrophysiologic excitability of nXII motoneurons themselves. We hypothesize that this mechanism is due to alterations in the ionic channels present in the membranes of these neurons. The Specific Aims of the second study are: 1) To determine biophysical membrane properties of nXII motoneurons at different postnatal ages and under conditions of prexisiting normoxia or hypoxia. And, 2) to determine which membrane ionic pathways are affected by rearing under conditions of pre- and postnatal hypoxia.